大肠杆菌16S核糖体RNA的特异性原位切割会干扰起始因子IF-1的功能。
Specific in situ cleavage of 16S ribosomal RNA of Escherichia coli interferes with the function of initiation factor IF-1.
作者信息
Baan R A, Duijfjes J J, van Leerdam E, van Knippenberg P H, Bosch L
出版信息
Proc Natl Acad Sci U S A. 1976 Mar;73(3):702-6. doi: 10.1073/pnas.73.3.702.
Abstract
Specific in situ cleavage of 16S rRNA of E. coli has been accomplished by in vitro treatment of 70S ribosomes ("tight couples") with the bacteriocin cloacin DF13. The defective ribosomes, which have fully lost their ability to sustain polypeptide synthesis, are still able to form initiation on complexes with MS2 RNA, but the kinetics are altered. This is apparently due to an improper functioning of initiation factor IF-1, for the defective ribosomal couples respond normally to dissociation by IF-3 but the dissociation is not stimulated by IF-1. The initiation complexes formed with defective ribosomes are fully reactive with puromycin. Their ability to bind alanyl-tRNA is reduced by about 50% at all concentrations of elongation factor Tu studied. Cleavage of the 16S rRNA, not the release of the terminal fragment from the ribosome, causes the block of protein synthesis and the aberrations observed during initiation and elongation.
摘要
通过用细菌素cloacin DF13对70S核糖体（“紧密偶联物”）进行体外处理，已实现对大肠杆菌16S rRNA的特异性原位切割。那些已完全丧失维持多肽合成能力的缺陷核糖体，仍能够与MS2 RNA形成起始复合物，但动力学发生了改变。这显然是由于起始因子IF-1功能异常所致，因为缺陷核糖体偶联物对IF-3介导的解离反应正常，但IF-1不会刺激这种解离。与缺陷核糖体形成的起始复合物与嘌呤霉素完全反应。在所研究的延伸因子Tu的所有浓度下，它们结合丙氨酰 - tRNA的能力降低了约50%。16S rRNA的切割，而非核糖体末端片段的释放，导致蛋白质合成受阻以及在起始和延伸过程中观察到的异常现象。
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Specific in situ cleavage of 16S ribosomal RNA of Escherichia coli interferes with the function of initiation factor IF-1.大肠杆菌16S核糖体RNA的特异性原位切割会干扰起始因子IF-1的功能。
Proc Natl Acad Sci U S A. 1976 Mar;73(3):702-6. doi: 10.1073/pnas.73.3.702.
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